Atherosclerosis is a progressive disease characterized by the thickening, hardening and loss of elasticity of inner artery walls. The pathologic process underlies most coronary heart disease (CHD) and strokes.
Since atherosclerosis is a leading cause of mortality and morbidity in the world, intense research efforts have been dedicated to the disease for the past two centuries. Many researchers have been focusing on the understanding of atherosclerosis mechanism and the development of efficient screening procedures [1, 2].
Since Anitschkow, N. stated that dietary cholesterol caused atherosclerosis in 1913, over the past five decades, lipid-lowering therapy has played a central role in the prevention and treatment of atherosclerosis-related CHD or stroke. This therapeutic method treats the elevated level of low-density lipoprotein (LDL) or cholesterol in blood as a primary cause in atherosclerosis [3]. In deciding whether a patient requires the therapy to prevent or to treat the disease, physicians usually rely heavily on measuring the LDL concentration in the patient's blood. The expert panels in the USA, Europe, UK and Canada have defined the guidelines of LDL level in serum [4-7]. It was reported that there were about 55 million American adults who had elevated level of LDL that warranted intervention [8]. The lipids hypothesis emphasizes a causal relationship between the elevated LDL level and disease. However, clinical evidences indicated that many individuals in the United States developed atherosclerosis-related CHD in the absence of abnormalities in the lipoprotein profile [9].
The recent method for diagnosing the disease is the so-called the measurement of C-reactive protein (CRP) concentration in blood plasma [9-10]. The method treats atherosclerosis as an inflammatory disease. In 1852, Rokitansky, C. V. suggested that small mural thrombi existed at the arterial wall, which led to plaques. In 1856, Virchow, R. stated that an early event in atherosclerosis was an inflammatory response to an injured arterial wall. In 1973, Ross, R. and Glomset, J. combined the two hypotheses and suggested the response-to-injury hypothesis [11]. The inflammatory hypothesis emphasizes inflammation as a primary cause in atherosclerosis [9-11]. The above-mentioned two major methods for diagnosing the disease are not mutually exclusive but they cannot be united.
In 1969, Caro, C. G., et al. found that atherosclerotic lesion occurred in areas experiencing low wall shear stress [12]. In 1980, Texon, M. developed a concept called hemodynamic basis of atherosclerosis [13]. In 1983, Friedman, M. H., et al. stated a causal relationship between arterial geometry and atherosclerosis [14]. Clinical and experimental evidences indicated that the elevated level of heart rate causes atherosclerosis [15-16]. In 1991, Schwartz, C. J., et al. suggested a unifying hypothesis that focused on lesion-prone arterial sites [17]. More recently, Wang, H. H. created analytical models of atherosclerosis [2]. Kruth, H. S. emphasized increased LDL uptake into arterial walls as a primary cause in atherosclerosis [18]. However, there is no screening method that is able to determine the effects of these risk factors on the disease.
Epidemiological studies stated that many risk factors influenced atherosclerosis, mainly including elevated LDL level, hypertension, smoking cigarette, family history, systemic inflammation such as rheumatoid arthritis, infectious agents such as Chlamydia pneumoniae, high-fat diet and emotion factors such as depression [3, 19]. However, the contributions of these risk factors to the disease cannot be combined using current screening methods, which result in limited reliable clinical screening capabilities. In recent review article entitled “atherosclerosis”, Lusis, A. J. points out that efficient screening procedures are urgently needed but they are unlikely to be available in the near future [19].